Evidence of a vicious cycle in glutamine synthesis and breakdown in pathogenesis of hepatic encephalopathy-thereapeutic perspectives

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F14%3A10209641" target="_blank" >RIV/00216208:11150/14:10209641 - isvavai.cz</a>

Výsledek na webu

<a href="http://link.springer.com/article/10.1007%2Fs11011-013-9428-9" target="_blank" >http://link.springer.com/article/10.1007%2Fs11011-013-9428-9</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s11011-013-9428-9" target="_blank" >10.1007/s11011-013-9428-9</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Evidence of a vicious cycle in glutamine synthesis and breakdown in pathogenesis of hepatic encephalopathy-thereapeutic perspectives

Popis výsledku v původním jazyce

The article provides evidence that a vicious cycle in glutamine synthesis and breakdown among tissues with high levels of glutamine synthetase (skeletal muscle, brain) and glutaminase (enetrocytes, kidneys) is activated in liver failure. These alterations may explain why therapies targeted to intestinal bacteria have only a limited effect on ammonia levels in patients with liver failure and indicate the needs of new therapeutic strategies focused on glutamine metabolism. The positive and adverse effectsof various nutritional and pharmacological strategies focused on glutamine metabolism in treatment of hyperammonemia and hepatice encephalopathy are discussed in the second part of the article. Attention is given to glutamine, glutamate, alpha-ketoglutarate, branched-chain amino acids, glutaminase inhibitors, and phenylbutyrate.

Název v anglickém jazyce

Evidence of a vicious cycle in glutamine synthesis and breakdown in pathogenesis of hepatic encephalopathy-thereapeutic perspectives

Popis výsledku anglicky

The article provides evidence that a vicious cycle in glutamine synthesis and breakdown among tissues with high levels of glutamine synthetase (skeletal muscle, brain) and glutaminase (enetrocytes, kidneys) is activated in liver failure. These alterations may explain why therapies targeted to intestinal bacteria have only a limited effect on ammonia levels in patients with liver failure and indicate the needs of new therapeutic strategies focused on glutamine metabolism. The positive and adverse effectsof various nutritional and pharmacological strategies focused on glutamine metabolism in treatment of hyperammonemia and hepatice encephalopathy are discussed in the second part of the article. Attention is given to glutamine, glutamate, alpha-ketoglutarate, branched-chain amino acids, glutaminase inhibitors, and phenylbutyrate.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Metabolic Brain Disease

ISSN

0885-7490

e-ISSN

—

Svazek periodika

29

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

9-17

Kód UT WoS článku

000331965900002

EID výsledku v databázi Scopus

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